Evidence map›Paper›PMID 34344968›Full record

ArticleScientific reports2021

MicroRNA-223 inhibits neutrophil extracellular traps formation through regulating calcium influx and small extracellular vesicles transmission.

Tsai-Ling Liao, Yi-Ming Chen, Kuo-Tung Tang, Po-Ku Chen, Hung-Jen Liu, Der-Yuan Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  14. Platelets in Alcohol-Associated Liver Disease: Interaction With Neutrophils.Cellular and molecular gastroenterology and hepatology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Tsai-Ling LiaoDepartment of Medical Research, Taichung Veterans General Hospital, Taichung, 407, Taiwan.
Yi-Ming Chen *Department of Medical Research, Taichung Veterans General Hospital, Taichung, 407, Taiwan.
Kuo-Tung Tang *Division of Allergy, Immunology and Rheumatology, Taichung Veterans General Hospital, Taichung, 407, Taiwan.
Po-Ku ChenRheumatology and Immunology Center, Department of Medicine, China Medical University Hospital, No. 2, Yude Road, Taichung, 40447, Taiwan.
Hung-Jen LiuRong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung, 402, Taiwan.
Der-Yuan ChenRheumatology and Immunology Center, Department of Medicine, China Medical University Hospital, No. 2, Yude Road, Taichung, 40447, Taiwan. dychen1957@gmail.com.
Taichung Veterans General Hospital · TWChina Medical University · TWChina Medical University Hospital · TWNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modulation of miRNAs and neutrophil extracellular traps (NETs) formation are both implicated in inflammatory disorders. Adult-onset Still's disease (AOSD) is a systemic autoinflammatory disease with neutrophilic leukocytosis and unknown etiology. Although the NETs formation is elevated in AOSD patients, the regulatory roles of miRNAs in NETs formation in AOSD remains unclear. We revealed that the circulating levels of IL-18, NETs, and miR-223 were significantly higher in active AOSD patients, compared with inactive AOSD patients or healthy controls (P < 0.005). Moreover, IL-18 increased calcium influx into neutrophils, which led to mitochondrial ROS (mROS) production and NETs formation. Elevated levels of NETs-DNA could induce miR-223 expression in neutrophils through activating Toll-like receptor 9. The upregulated miR-223 expression in neutrophils suppressed mROS production by blocking calcium influx, and subsequently inhibited IL-18-mediated NETs formation. Besides, the increased neutrophil-derived exosomal miR-223 levels were observed in active AOSD patients compared with healthy controls (P < 0.005). Our in vitro assays demonstrated that the neutrophil-derived small extracellular vesicles carried miR-223, which could repress IL-18 production in macrophages. Together, these results suggest a fine-tuned mechanism between inflammatory (IL-18 induced NETs) and anti-inflammatory (miR-223) factors in AOSD. MiR-223, mROS inhibitors, and calcium channel blockers are the potential therapeutics for autoinflammatory diseases such as AOSD.

Indexed as

CalciumDisease SusceptibilityExtracellular TrapsExtracellular VesiclesGene Expression RegulationHumansInterleukin-18MacrophagesMicroRNAsMitochondriaNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesStill's Disease, Adult-OnsetCalciumInterleukin-18MicroRNAsMIR223, humanNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanReactive Oxygen Species

Identifiers

PMID34344968
PMCPMC8333426
OpenAlexW3189719673

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.